Nutrition usually makes a small but potentially valuable contribution to successful performance in elite athletes, and dietary supplements can make a minor contribution to this nutrition program. Nonetheless, supplement use is widespread at all levels of sport. Products described as supplements target different issues, including the management of micronutrient deficiencies, supply of convenient forms of energy and macronutrients, and provision of direct benefits to performance or indirect benefits such as supporting intense training regimens. The appropriate use of some supplements can offer benefits to the athlete, but others may be harmful to the athlete's health, performance, and/or livelihood and reputation if an anti-doping rule violation results. A complete nutritional assessment should be undertaken before decisions regarding supplement use are made. Supplements claiming to directly or indirectly enhance performance are typically the largest group of products marketed to athletes, but only a few (including caffeine, creatine, specific buffering agents and nitrate) have good evidence of benefits. However, responses are affected by the scenario of use and may vary widely between individuals because of factors that include genetics, the microbiome, and habitual diet. Supplements intended to enhance performance should be thoroughly trialed in training or simulated competition before implementation in competition. Inadvertent ingestion of substances prohibited under the anti-doping codes that govern elite sport is a known risk of taking some supplements. Protection of the athlete's health and awareness of the potential for harm must be paramount, and expert professional opinion and assistance is strongly advised before embarking on supplement use.

Nutrition usually makes a small but potentially valuable contribution to successful performance in elite athletes, and dietary supplements can make a minor contribution to this nutrition programme. Nonetheless, supplement use is widespread at all levels of sport. Products described as supplements target different issues, including (1) the management of micronutrient deficiencies, (2) supply of convenient forms of energy and macronutrients, and (3) provision of direct benefits to performance or (4) indirect benefits such as supporting intense training regimens. The appropriate use of some supplements can benefit the athlete, but others may harm the athlete’s health, performance, and/or livelihood and reputation (if an antidoping rule violation results). A complete nutritional assessment should be undertaken before decisions regarding supplement use are made. Supplements claiming to directly or indirectly enhance performance are typically the largest group of products marketed to athletes, but only a few (including caffeine, creatine, specific buffering agents and nitrate) have good evidence of benefits. However, responses are affected by the scenario of use and may vary widely between individuals because of factors that include genetics, the microbiome and habitual diet. Supplements intended to enhance performance should be thoroughly trialled in training or simulated competition before being used in competition. Inadvertent ingestion of substances prohibited under the antidoping codes that govern elite sport is a known risk of taking some supplements. Protection of the athlete’s health and awareness of the potential for harm must be paramount; expert professional opinion and assistance is strongly advised before an athlete embarks on supplement use.

Iron is utilised by the body for oxygen transport and energy production, and is therefore essential to athletic performance. Commonly, athletes are diagnosed as iron deficient, however, contrasting evidence exists as to the severity of deficiency and the effect on performance. Iron losses can result from a host of mechanisms during exercise such as hemolysis, hematuria, sweating and gastrointestinal bleeding. Additionally, recent research investigating the anemia of inflammation during states of chronic disease has allowed us to draw some comparisons between unhealthy populations and athletes. The acute-phase response is a well-recognised reaction to both exercise and disease. Elevated cytokine levels from such a response have been shown to increase the liver production of the hormone Hepcidin. Hepcidin up-regulation has a negative impact on the iron transport and absorption channels within the body, and may explain a potential new mechanism behind iron deficiency in athletes. This review will attempt to explore the current literature that exits in this new area of iron metabolism and exercise.

Iron plays a significant role in the body, and is specifically important to athletes, since it is a dominant feature in processes such as oxygen transport and energy metabolism. Despite its importance, athlete populations, especially females and endurance athletes, are commonly diagnosed with iron deficiency, suggesting an association between sport performance and iron regulation. Although iron deficiency is most common in female athletes (~15-35% athlete cohorts deficient), approximately 5-11% of male athlete cohorts also present with this issue. Furthermore, interest has grown in the mechanisms that influence iron absorption in athletes over the last decade, with the link between iron regulation and exercise becoming a research focus. Specifically, exercise-induced increases in the master iron regulatory hormone, hepcidin, has been highlighted as a contributing factor towards altered iron metabolism in athletes. To date, a plethora of research has been conducted, including investigation into the impact that sex hormones, diet (e.g. macronutrient manipulation), training and environmental stress (e.g. hypoxia due to altitude training) have on an athlete's iron status, with numerous recommendations proposed for consideration. This review summarises the current state of research with respect to the aforementioned factors, drawing conclusions and recommendations for future work.

With empirical research on team resilience on the rise, there is a need for an integrative conceptual model that delineates the essential elements of this concept and offers a heuristic for the integration of findings across studies. To address this need, we propose a multilevel model of team resilience that originates in the resources of individual team members and emerges as a team-level construct through dynamic person-situation interactions that are triggered by adverse events. In so doing, we define team resilience as an emergent outcome characterized by the trajectory of a team's functioning, following adversity exposure, as one that is largely unaffected or returns to normal levels after some degree of deterioration in functioning. This conceptual model offers a departure point for future work on team resilience and reinforces the need to incorporate inputs and process mechanisms inherent within dynamic interactions among individual members of a team. Of particular, importance is the examination of these inputs, process mechanisms and emergent states, and outcomes over time, and in the context of task demands, objectives, and adverse events. Practitioner pointsTeam resilience as a dynamic, multilevel phenomenon requires clarity on the individual-and team-level factors that foster its emergence within occupational and organizational settings. An understanding of the nature (e.g., timing, chronicity) of adverse events is key to studying and intervening to foster team resilience within occupational and organizational settings.

This study explored the relationship between serum ferritin and hepcidin in athletes. Baseline serum ferritin levels of 54 athletes from the control trial of five investigations conducted in our laboratory were considered; athletes were grouped according to values <30 μg/L (SF<30), 30–50 μg/L (SF30–50), 50–100 μg/L (SF50–100), or >100 μg/L (SF>100). Data pooling resulted in each athlete completing one of five running sessions: (1) 8×3 min at 85% vVO2peak; (2) 5×4 min at 90% vVO2peak; (3) 90 min continuous at 75% vVO2peak; (4) 40 min continuous at 75% vVO2peak; (5) 40 min continuous at 65% vVO2peak. Athletes from each running session were represented amongst all four groups; hence, the mean exercise duration and intensity were not different (p>0.05). Venous blood samples were collected pre-, post- and 3 h post-exercise, and were analysed for serum ferritin, iron, interleukin-6 (IL-6) and hepcidin-25. Baseline and post-exercise serum ferritin levels were different between groups (p<0.05). There were no group differences for pre- or post-exercise serum iron or IL-6 (p>0.05). Post-exercise IL-6 was significantly elevated compared to baseline within each group (p<0.05). Pre- and 3 h post-exercise hepcidin-25 was sequentially greater as the groups baseline serum ferritin levels increased (p<0.05). However, post-exercise hepcidin levels were only significantly elevated in three groups (SF30–50, SF50–100, and SF>100; p<0.05). An athlete's iron stores may dictate the baseline hepcidin levels and the magnitude of post-exercise hepcidin response. Low iron stores suppressed post-exercise hepcidin, seemingly overriding any inflammatory-driven increases.

Urinary hepcidin, inflammation, and iron metabolism were examined during the 24 hr after exercise. Eight moderately trained athletes (6 men, 2 women) completed a 60-min running trial (15-min warm-up at 75-80% HR(peak) + 45 min at 85-90% HR(peak)) and a 60-min trial of seated rest in a randomized, crossover design. Venous blood and urine samples were collected pretrial, immediately posttrial, and at 3, 6, and 24 hr posttrial. Samples were analyzed for interleukin-6 (IL-6), C-reactive protein (CRP), serum iron, serum ferritin, and urinary hepcidin. The immediate postrun levels of IL-6 and 24-hr postrun levels of CRP were significantly increased from baseline (6.9 and 2.6 times greater, respectively) and when compared with the rest trial (p < or = .05). Hepcidin levels in the run trial after 3, 6, and 24 hr of recovery were significantly greater (1.7-3.1 times) than the pre- and immediate postrun levels (p < or = .05). This outcome was consistent in all participants, despite marked variation in the magnitude of rise. In addition, the 3-hr postrun levels of hepcidin were significantly greater than at 3 hr in the rest trial (3.0 times greater, p < or = .05). Hepcidin levels continued to increase at 6 hr postrun but failed to significantly differ from the rest trial (p = .071), possibly because of diurnal influence. Finally, serum iron levels were significantly increased immediately postrun (1.3 times, p < or = .05). The authors concluded that high-intensity exercise was responsible for a significant increase in hepcidin levels subsequent to a significant increase in IL-6 and serum iron.

Purpose:The effect of crushed ice ingestion as a precooling method on 40-km cycling time trial (CTT) performance was investigated.Methods:Seven trained male subjects underwent a familiarization trial and two experimental CTT which were preceded by 30 min of either crushed ice ingestion (ICE) or tap water (CON) consumption amounting to 6.8 g⋅kg-1 body mass. The CTT required athletes to complete 1200 kJ of work on a wind-braked cycle ergometer. During the CTT, gastrointestinal (Tgi) and skin (Tsk) temperatures, cycling time, power output, heart rate (HR), blood lactate (BLa), ratings of perceived exertion (RPE) and thermal sensation (RPTS) were measured at set intervals of work.Results:Precooling lowered the Tgi after ICE significantly more than CON (36.74 ± 0.67°C vs 37.27 ± 0.24°C, P < .05). This difference remained evident until 200 kJ of work was completed on the bike (37.43 ± 0.42°C vs 37.64 ± 0.21°C). No significant differences existed between conditions at any time point for Tsk, RPE or HR (P > .05). The CTT completion time was 6.5% faster in ICE when compared with CON (ICE: 5011 ± 810 s, CON: 5359 ± 820 s, P < .05).Conclusions:Crushed ice ingestion was effective in lowering Tgi and improving subsequent 40-km cycling time trial performance. The mechanisms for this enhanced exercise performance remain to be clarified.